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Associations between fetal heart rate variability and umbilical cord occlusions‐induced neural injury: An experimental study in a fetal sheep model
INTRODUCTION: This study evaluated the association between fetal heart rate variability (HRV) and the occurrence of hypoxic–ischemic encephalopathy in a fetal sheep model. MATERIAL AND METHODS: The experimental protocol created a hypoxic condition with repeated cord occlusions in three phases (A, B,...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9564451/ https://www.ncbi.nlm.nih.gov/pubmed/35502642 http://dx.doi.org/10.1111/aogs.14352 |
Sumario: | INTRODUCTION: This study evaluated the association between fetal heart rate variability (HRV) and the occurrence of hypoxic–ischemic encephalopathy in a fetal sheep model. MATERIAL AND METHODS: The experimental protocol created a hypoxic condition with repeated cord occlusions in three phases (A, B, C) to achieve acidosis to pH <7.00. Hemodynamic, gasometric and HRV parameters were analyzed during the protocol, and the fetal brain, brainstem and spinal cord were assessed histopathologically 48 h later. Associations between the various parameters and neural injury were compared between phases A, B and C using Spearman's rho test. RESULTS: Acute anoxic–ischemic brain lesions in all regions was present in 7/9 fetuses, and specific neural injury was observed in 3/9 fetuses. The number of brainstem lesions correlated significantly and inversely with the HRV fetal stress index (r = −0.784; p = 0.021) in phase C and with HRV long‐term variability (r = −0.677; p = 0.045) and short‐term variability (r = −0.837; p = 0.005) in phase B. The number of neurological lesions did not correlate significantly with other markers of HRV. CONCLUSIONS: Neural injury caused by severe hypoxia was associated with HRV changes; in particular, brainstem damage was associated with changes in fetal‐specific HRV markers. |
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